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Biomedical subjects

R Saracci

Publications and source records attributed to R Saracci.

At least 37 records · Page 2Linked to original sources
PubMed1990

The diet and cancer hypothesis: current trends.

The current decade has witnessed an increasing interest in the diet-cancer issue as a central one for public health. Notwithstanding a substantial amount of epidemiological investigations, firm evidence of carcinogenicity exists only for alcoholic beverages with respect to cancers at several sites, and for aflatoxin with respect to liver cancer; also, the relation is established between diet related excess of energy intake, as translated into obesity, and cancer of endometrium and gallbladder. For a number of other dietary factors the evidence for a causal or protective role still remains at a presumptive level (e.g. intake of fresh vegetables and fruits with respect to cancers at several sites), or is still frankly open to debate (e.g. fat with respect to breast and colon cancer). Methodological inadequacies in past studies have been identified and clearer results should derive in the coming decade from epidemiological investigations substantially improved in methodology, particularly from the long-term prospective studies as now planned by the International Agency for Research on Cancer. Fortunately for cancer prevention, such dietary advice as can be derived from the highly incomplete and unsatisfactory knowledge on the role of dietary factors on cancer, turns out to be in broad agreement with the advice aimed at preventing other major diseases such as ischaemic heart disease and hypertension. This allows the issuing of a set of simple but important 'prudent diet' recommendations.

Body Weight↗
PubMed1990

Pulmonary lipid peroxidation in cigarette smokers and lung cancer patients.

Lipid peroxidation (LPO) was studied in lung tissues of patients with lung cancer (LC, n = 37) or nonlung cancer (NLC, n = 13) and its relationships with the smoking habits and the degree of airway obstruction were investigated. Specimens of peripheral lung parenchyma, free of tumor tissue, were taken and the malondialdehyde (MDA) content was measured in the S-12 fractions. Airway obstruction was assessed by flow-volume curves, and data were expressed as percentage of the predicted values. Cigarettes smoked were expressed as pack-years. The patients with LC and NLC did not differ by MDA content, age, and number of pack-years. On the contrary, FEF75-85 and MEF75 were significantly lower in LC than in NLC patients (p less than 0.05). The MDA content was inversely correlated to number of days patients had refrained from smoking (r = -0.66, p less than 0.001). The MDA content was higher in recent smokers (ie, people smoking during the last 30 days before surgery) than in the other patients (0.136 +/- 0.007 vs 0.116 +/- 0.007 mumol/g of tissue, p less than 0.05) and, by considering only recent smokers, MDA content was higher in LC patients (0.144 +/- 0.008 mumol/g of tissue) than in NLC patients (0.113 +/- 0.014 mmol/g tissue, p = 0.059). When patients were divided into "high MDA" and "low MDA" groups, MEF75 was much lower in the high MDA group (35.1 +/- 3.4 percent) than in the low MDA group (55.1 +/- 8.1 percent) (p less than 0.01). These results suggest the following: (1) enhanced level of prooxidant state in the lungs is associated with recent cigarette smoking; (2) LC patients may be more prone than respective NLC patients to oxidative stress; (3) MDA level and degree of small airway obstruction were associated and differed between LC and NLC patients even though these groups did not differ in the percentage of recent smokers; and (4) a common free-radical mediated pathway may be active for both LC and small airway obstruction.

Glutathione↗
PubMed1990

Epidemiologic evidence on the relationship between formaldehyde exposure and cancer.

Over 30 epidemiologic studies have evaluated cancer risks associated with formaldehyde exposure. Excesses were reported for several sites, leukemia and cancers of the nasal cavities, nasopharynx, lung, and brain generating the greatest interest. The excesses of leukemia and brain and colon cancer found among professionals may not be related to formaldehyde exposure, since similar excesses were not observed among industrial workers. Inconsistencies among and within studies impede assigning formaldehyde a convincing causal role for the excesses of lung cancer found among industrial workers. A causal role for formaldehyde is the most probable for cancers of the nasopharynx and, to a less extent, the nasal cavities. Evidence of exposure-response relationships, the fact that direct contact with formaldehyde may occur at these upper respiratory sites, and the consistency of these findings with experimental studies make this assumption highly probable.

Brain Neoplasms↗
PubMed1989

Passive smoking and lung cancer: current evidence and ongoing studies at the International Agency for Research on Cancer.

The evidence available from 3 cohort and 11 case-control studies investigating the relationship between exposure to environmental tobacco smoke (ETS) and lung cancer in non-smokers is reviewed. While it appears most likely that a causal relationship exists, the size of the effect, under different circumstances of exposures, remains to be accurately estimated. This requires studies using valid instruments (e.g., questionnaires) to quantitate exposures, and free as far as possible from biases. An investigation addressing this point is in progress under the coordination of the International Agency for Research on Cancer.

Female↗
PubMed1989

Carcinogen metabolism studies in human bronchial and lung parenchymal tissues.

The pulmonary metabolism of xenobiotics was investigated by measuring the glutathione content and the activity of the aryl hydrocarbon hydroxylase, epoxide hydrolase, glutathione S-transferase, and uridine 5' -diphosphoglucuronosyl transferase enzymes in S-12 fractions of bronchial tree and peripheral lung parenchyma obtained at surgery from 21 patients. In parallel, the same preparations were used to assess either the activation of promutagens, i.e., benzo(a)pyrene, 2-aminofluorene, cyclophosphamide, and a cigarette smoke condensate, to metabolites reverting his- Salmonella typhymurium strains, or the decrease of direct-acting mutagens, i.e., sodium dichromate, 4-nitroquinoline N-oxide, epichlorohydrin, and ICR 191. As compared to bronchus preparations, parenchymal preparations contained considerably higher concentrations of reduced glutathione, had a significantly higher epoxide hydrolase activity, and, as assessed by means of a quantitative index, were more efficient in activating 2-aminofluorene and in reducing the mutagenicity of dichromate and 4-nitroquinoline N-oxide. These data may suggest that parenchymal lung tissue is more capable than bronchial tissue to detoxify reactive intermediates of xenobiotics, possibly explaining the greater susceptibility of bronchi to cigarette smoke-induced cancers.

4-Nitroquinoline-1-oxide↗
PubMed1989

Relation of environmental exposure to erionite fibres to risk of respiratory cancer.

During the period 1979-1983, IARC, in collaboration with the Department of Chest Diseases of Hacettepe University in Ankara and the MRC Pneumoconiosis Unit in Penarth, conducted an epidemiological and environmental survey in 4 villages in central Turkey affected by a high incidence of mesothelial tumours. Recent data point to erionite, a zeolite fibre, as the most plausible etiological agent. From animal experiments, erionite appears to be the most powerful carcinogenic fibre so far known. During the study period, 17 pleural mesotheliomas and 7 lung cancer cases have been reported among the villagers. These cancer cases are analysed in relation to exposure to fibres. We assume exposure to occur from birth onwards and therefore consider duration of exposure equal to age. On this basis, the incidence of mesothelial and lung tumours is analysed in relation to age and cumulative exposure to fibres computed using the airborne fibre levels measured during the survey.

Adult↗
PubMed1989

Effects on health of non-occupational exposure to airborne mineral fibres.

The most prominent potential marker of disease-related non-occupational exposure to mineral fibres is mesothelioma. Although many cases of mesothelioma have resulted from occupational exposure to asbestos, some have been associated with para-occupational domestic and/or neighbourhood exposure and have been reported in case series, case-control studies and a cohort study among non-occupationally exposed subjects. However, little information is available on mesothelioma as a direct consequence of general environmental asbestos exposure. Such cases of mesothelioma related to non-occupational exposure to asbestos as have occurred to date are likely to have resulted from past exposures much higher than those prevailing at the present time (in the developed countries); numbers will therefore probably decrease in the future. Very high rates of mesothelioma have been reported as a result of exposure to erionite. No studies are available on the effects of non-occupational exposure to man-made mineral fibres but, among occupationally exposed workers, a risk of mesothelioma is not apparent. There are suggestions of raised lung cancer rates among household contacts of asbestos workers and among individuals exposed to erionite. Non-malignant parenchymal and pleural abnormalities have been observed in subjects exposed non-occupationally to asbestos and erionite, but these are not necessarily associated with malignant lesions. Quantitative risk estimates of adverse effects on health have not been derived from these studies, essentially because of the absence of fibre exposure measurements.

Air Pollutants↗
PubMed1987

Epidemiological and environmental evidence of the health effects of exposure to erionite fibres: a four-year study in the Cappadocian region of Turkey.

An environmental and epidemiological study has been carried out in Central Cappadocia, Turkey, aiming at investigating the relationship between exposure to naturally occurring erionite fibres and the reported high incidence of malignant mesotheliomas. Airborne fibre levels are generally low but show a higher proportion of erionite fibres in the villages affected by malignant disease than in a control village. The same pattern is confirmed by analysis of the fibre content in lung tissues of sheep from several villages, both affected and unaffected by malignant disease. The 3 villages with the highest proportion of erionite fibres have high rates of malignant pleural mesothelioma, malignant peritoneal mesothelioma and lung cancer. No case of malignancy for the same sites has been reported during the study period from the control village. The relationships between these findings and their consistency with the results from experimental studies indicate erionite fibres as a carcinogenic agent, although some aspects of the exposure are not fully clarified.

Adult↗
PubMed1985

[Markers of exposure and early lesions in cancer epidemiology].

The biological markers of risk can be separated into two categories: markers of exposure to a specific substance, based on several biochemical, physical and immunological methods (usually able to measure the absorbed dose); markers of early lesions which usually are not specific for a particular substance and do not estimate the dose of exposure. In epidemiological research on cancer etiology, biological markers have a different role according to whether cases are subjects with early lesions or with invasive cancers. The first approach has the advantage of shortening the observation time between exposure and the appearance of a biological effect. On the other hand, the biological relevance of the study could be limited due to the non univocal relation between early lesions and cancer. With the second approach, invasive cancer can be related to specific markers of exposure (this would permit to draw direct inference on disease etiology) or to markers of early lesions (etiological interpretation in this case would be less straightforward). The two approaches should be considered in the frame of two basic problems: What is the advantage of measuring exposure at the individual level? What is the advantage of a biological marker as compared to traditional epidemiological methods? With studies at the group level the correlation between exposure variables and disease frequency can be estimated. Nevertheless only studies at the individual level can exclude the fact that the observed correlation is due to an artefact. In this case we are left with the second question and many answers are possible.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Hepatocellular↗